Chapter 6: Sleep
Brain Activity during Sleep
Sleep disorders
How is sleep regulated?
The Sleep-Wakefulness Cycle
Lack of sleep increases the risk of many health problems including:
Diabetes
Cardiovascular disease
Heart attacks
Stroke
Depression
High Blood Pressure/Hypertension
Obesity
Infections
Sleep is made of several different stages that are accompanied by daily rhythms in hormones, body temperature, etc.
Sleep disorders are one of the least recognized sources of disease, disability, and death
Electroencephalography (EEG): the measurement of electrical activity in different parts of the brain and the recording of such activity as a visual trace (on paper or on an oscilloscope screen).
One sleep cycle is approximately 90 minutes
Each night, the brain progresses through a series of stages when brain waves slow down for 60 minutes in NREM (non-rapid eye movement) sleep
This is accompanied by the relaxation of muscles and eyes
Heart rate, Blood pressure, and body temperature fall
If awakened in this stage of sleep, most people only recall fragments of thought
NREM sleep: sleep where the eyes do not rapidly move
Over the next half-hour, brain activity changes to REM sleep
REM (Rapid Eye Movement) sleep: sleep characterized by the random rapid movement of the eyes when derams also occur
Characterized by neocortical (in the neocortex) EEG waves similar to those when a person is awake
REM is accompanied by atonia
Atonia: paralysis of muscle
Dreaming occurs only in REM sleep
The first REM period lasts 10-15 min
Over the course of one’s lifetime: slow-wave sleep time decreases & REM time increases
Overall sleeping time at different life stages:
Infants: up to 18 hrs
Older adults: 6-7 hrs
Less time sleeping in general and in slow wave sleep specifically
Insomnia: the most common sleep disorder where individuals have trouble falling asleep
Some people have problems falling asleep, some wake up in the middle of the night and can’t fall asleep again
Sleeping drugs do not help because they suppress slow-wave sleep and aren’t effective in keeping people asleep
Many common disorders disrupt deeper stages of sleep
Excessive daytime sleepiness has many causes
Obstructive Sleep Apnea: airway muscles relax and close airway causing difficulty breathing
individual wakes up without entering deeper stages of slow-wave sleep.
Causes high blood pressure and increases the risk of heart attack
more daytime sleepiness
Periodic Limb Movements: intermittent jerks of the legs or arms that occur as individual enters slow wave sleep and cause arousal from sleep.
REM behavior disorder: occurs when muscles fail to become paralyzed during REM sleep
Act out dreams by getting up and moving around.
Can be very disruptive.
Both periodic limb movements and REM behavior disorder are more common in people with Parkinson’s disease.
Can be treated with drugs for Parkinson’s or with a benzodiazepine called clonazepam
Narcolepsy: mechanisms controlling transitions into sleep (particularly REM sleep) don’t work.
Narcolepsy is caused by the loss of nerve cells in lateral hypothalamus that contain orexin/hypocretin.
Have sleep attacks during day (suddenly fall asleep).
Hypnagogic hallucination: individuals tend to enter REM sleep very quickly and enter dreaming state while partially awake
Cataplexy: loss of muscle tone similar to what happens in REM sleep but occurs when the individual is still awake
Wakefulness is maintained by systems in the upper brainstem and hypothalamus
Neurons here use acetylcholine, norepinephrine, serotonin, glutamate to connect with the forebrain
Neurons in the hypothalamus use orexin and some contain histamine
Thalamus and basal forebrain activation by acetylcholine is very important too
basal means “closest to midbrain/base”
Level of alertness can be shown in an activated low-volt EEG
Arousing systems are less active in non-REM sleep
Transmission of information to the thalamus is limited
Ventrolateral preoptic (VLPO) nucleus: area in the brain that causes suppression of arousal systems
VLPO nucleus neurons have the inhibitors galanin and GABA
Damage to the VLPO area produces irreversible insomnia
In REM sleep, there is an internally activated brain and EEG but the external input is suppressed
Internal activation comes from cyclically active REM sleep generator neurons in the brainstem
Signals from neurons cause the excitation of the forebrain
Leads to rapid eye movements & muscle suppression
Forebrain excitation driving force behind dreams of REM sleep
Motor cortex neurons fire as rapidly during REM sleep as during waking movement
Explains movement coinciding with dreams
Periodic recurrence of REM sleep
REM sleep occurs every 90 min during sleep
This is caused by on-and-off switching of REM-generators (acetylcholine, glutamate) and REM-suppressors (norepinephrine, serotonin, GABA)
2 determining factors for sleepiness:
Circadian system: Monitoring the time of day/night
Homeostatic system: monitoring how long the person is awake
Circadian system is regulated by the suprachiasmatic nucleus
Suprachiasmatic nucleus: a small group of cells in the hypothalamus serving as the master clock
It expresses clock proteins that go through a biochemical cycle of approximately 24 hrs
This sets the pace for daily cycles of activity, sleep hormone release, etc.
The suprachiasmatic nucleus also receives input from the retina
The clock can be reset by light so it is linked to the outside day-night cycle
Also provides information to the subparaventricular nucleus → dorsomedial nucleus → VLPO and orexin neurons
Orexin: an excitatory signal to arousal system especially norepinephrine neurons
Orexin activation plays role in preventing transitions into REM sleep during the day
Arousal mediated by orexin and activation of norepinephrine neurons in the locus coeruleus
Locus coeruleus: a lateral part of brain stem that has norepinephrine producing neurons that mediate arousal along with orexin
The homeostatic system responds to longer wake periods by increasing the urge to sleep
The longer a person is awake, the greater the likelihood of an increase in sleep-inducing factors
Adenosine: a very important sleep promotor
More adenosine means increased sleepiness
Adenosine release starts in the basal forebrain and spreads to the rest of the cortex
Increased adenosine levels slow down cellular activity and diminish arousal
Adenosine levels decrease during sleep
Brain adenosine may be produced by ATP breakdown over the course of wakefulness
Neuron activity decreases and adenosine levels decline in non-REM sleep
ATP levels increase during sleep
Brain Activity during Sleep
Sleep disorders
How is sleep regulated?
The Sleep-Wakefulness Cycle
Lack of sleep increases the risk of many health problems including:
Diabetes
Cardiovascular disease
Heart attacks
Stroke
Depression
High Blood Pressure/Hypertension
Obesity
Infections
Sleep is made of several different stages that are accompanied by daily rhythms in hormones, body temperature, etc.
Sleep disorders are one of the least recognized sources of disease, disability, and death
Electroencephalography (EEG): the measurement of electrical activity in different parts of the brain and the recording of such activity as a visual trace (on paper or on an oscilloscope screen).
One sleep cycle is approximately 90 minutes
Each night, the brain progresses through a series of stages when brain waves slow down for 60 minutes in NREM (non-rapid eye movement) sleep
This is accompanied by the relaxation of muscles and eyes
Heart rate, Blood pressure, and body temperature fall
If awakened in this stage of sleep, most people only recall fragments of thought
NREM sleep: sleep where the eyes do not rapidly move
Over the next half-hour, brain activity changes to REM sleep
REM (Rapid Eye Movement) sleep: sleep characterized by the random rapid movement of the eyes when derams also occur
Characterized by neocortical (in the neocortex) EEG waves similar to those when a person is awake
REM is accompanied by atonia
Atonia: paralysis of muscle
Dreaming occurs only in REM sleep
The first REM period lasts 10-15 min
Over the course of one’s lifetime: slow-wave sleep time decreases & REM time increases
Overall sleeping time at different life stages:
Infants: up to 18 hrs
Older adults: 6-7 hrs
Less time sleeping in general and in slow wave sleep specifically
Insomnia: the most common sleep disorder where individuals have trouble falling asleep
Some people have problems falling asleep, some wake up in the middle of the night and can’t fall asleep again
Sleeping drugs do not help because they suppress slow-wave sleep and aren’t effective in keeping people asleep
Many common disorders disrupt deeper stages of sleep
Excessive daytime sleepiness has many causes
Obstructive Sleep Apnea: airway muscles relax and close airway causing difficulty breathing
individual wakes up without entering deeper stages of slow-wave sleep.
Causes high blood pressure and increases the risk of heart attack
more daytime sleepiness
Periodic Limb Movements: intermittent jerks of the legs or arms that occur as individual enters slow wave sleep and cause arousal from sleep.
REM behavior disorder: occurs when muscles fail to become paralyzed during REM sleep
Act out dreams by getting up and moving around.
Can be very disruptive.
Both periodic limb movements and REM behavior disorder are more common in people with Parkinson’s disease.
Can be treated with drugs for Parkinson’s or with a benzodiazepine called clonazepam
Narcolepsy: mechanisms controlling transitions into sleep (particularly REM sleep) don’t work.
Narcolepsy is caused by the loss of nerve cells in lateral hypothalamus that contain orexin/hypocretin.
Have sleep attacks during day (suddenly fall asleep).
Hypnagogic hallucination: individuals tend to enter REM sleep very quickly and enter dreaming state while partially awake
Cataplexy: loss of muscle tone similar to what happens in REM sleep but occurs when the individual is still awake
Wakefulness is maintained by systems in the upper brainstem and hypothalamus
Neurons here use acetylcholine, norepinephrine, serotonin, glutamate to connect with the forebrain
Neurons in the hypothalamus use orexin and some contain histamine
Thalamus and basal forebrain activation by acetylcholine is very important too
basal means “closest to midbrain/base”
Level of alertness can be shown in an activated low-volt EEG
Arousing systems are less active in non-REM sleep
Transmission of information to the thalamus is limited
Ventrolateral preoptic (VLPO) nucleus: area in the brain that causes suppression of arousal systems
VLPO nucleus neurons have the inhibitors galanin and GABA
Damage to the VLPO area produces irreversible insomnia
In REM sleep, there is an internally activated brain and EEG but the external input is suppressed
Internal activation comes from cyclically active REM sleep generator neurons in the brainstem
Signals from neurons cause the excitation of the forebrain
Leads to rapid eye movements & muscle suppression
Forebrain excitation driving force behind dreams of REM sleep
Motor cortex neurons fire as rapidly during REM sleep as during waking movement
Explains movement coinciding with dreams
Periodic recurrence of REM sleep
REM sleep occurs every 90 min during sleep
This is caused by on-and-off switching of REM-generators (acetylcholine, glutamate) and REM-suppressors (norepinephrine, serotonin, GABA)
2 determining factors for sleepiness:
Circadian system: Monitoring the time of day/night
Homeostatic system: monitoring how long the person is awake
Circadian system is regulated by the suprachiasmatic nucleus
Suprachiasmatic nucleus: a small group of cells in the hypothalamus serving as the master clock
It expresses clock proteins that go through a biochemical cycle of approximately 24 hrs
This sets the pace for daily cycles of activity, sleep hormone release, etc.
The suprachiasmatic nucleus also receives input from the retina
The clock can be reset by light so it is linked to the outside day-night cycle
Also provides information to the subparaventricular nucleus → dorsomedial nucleus → VLPO and orexin neurons
Orexin: an excitatory signal to arousal system especially norepinephrine neurons
Orexin activation plays role in preventing transitions into REM sleep during the day
Arousal mediated by orexin and activation of norepinephrine neurons in the locus coeruleus
Locus coeruleus: a lateral part of brain stem that has norepinephrine producing neurons that mediate arousal along with orexin
The homeostatic system responds to longer wake periods by increasing the urge to sleep
The longer a person is awake, the greater the likelihood of an increase in sleep-inducing factors
Adenosine: a very important sleep promotor
More adenosine means increased sleepiness
Adenosine release starts in the basal forebrain and spreads to the rest of the cortex
Increased adenosine levels slow down cellular activity and diminish arousal
Adenosine levels decrease during sleep
Brain adenosine may be produced by ATP breakdown over the course of wakefulness
Neuron activity decreases and adenosine levels decline in non-REM sleep
ATP levels increase during sleep